title: Facilitation of synaptic transmission in the anterior cingulate cortex in viscerally hypersensitive rats.
abstract: Electrophysiological studies have shown the enhanced response of anterior cingulate cortex (ACC) to colorectal distension in viscerally hypersensitive (VH) rats, which can be observed up to 7 weeks following colonic anaphylaxis, independent of colon inflammation, suggesting a mechanism for learning and triggering of pain memories in the ACC neuronal circuitry. Activity-dependent plasticity in synaptic strength may serve as a key mechanism that reflects cortical plasticity. However, only a few reports have indicated the synaptic plasticity of ACC in vivo. In the present study, electrophysiological recording showed long-lasting potentiation of local field potential in the medial thalamus (MT)-ACC synapses in VH rats. Theta burst stimulation in the MT reliably induced long-term potentiation in the MT-ACC pathway in normal rats, but was occluded in the VH state. Further, repeated tetanization of MT increased ACC neuronal activity and visceral pain responses of normal rats, mimicking VH rats. In conclusion, we demonstrated for the first time that visceral hypersensitivity is associated with alterations of synaptic plasticity in the ACC. The ACC synaptic strengthening in chronic visceral pain may engage signal transduction pathways that are in common with those activated by electrical stimulation, and serves as an attractive cellular model of functional visceral pain.
authors.affiliation: Neuroscience Laboratory, Department of Biology and Chemistry, Centre for Biosystems, Neuroscience, and Nanotechnology, City University of Hong Kong, Hong Kong, China Key Laboratory of Biochip Technology, Shenzhen Biotech and Health Centre, City University of Hong Kong, Shenzhen 518057, PR China.
authors.forename: Jun
authors.initials: J
authors.lastname: Wang
authors.affiliation: Neuroscience Laboratory, Department of Biology and Chemistry, Centre for Biosystems, Neuroscience, and Nanotechnology, City University of Hong Kong, Hong Kong, China Key Laboratory of Biochip Technology, Shenzhen Biotech and Health Centre, City University of Hong Kong, Shenzhen 518057, PR China.
authors.forename: Xu
authors.initials: X
authors.lastname: Zhang
authors.affiliation: Neuroscience Laboratory, Department of Biology and Chemistry, Centre for Biosystems, Neuroscience, and Nanotechnology, City University of Hong Kong, Hong Kong, China Key Laboratory of Biochip Technology, Shenzhen Biotech and Health Centre, City University of Hong Kong, Shenzhen 518057, PR China.
authors.forename: Bing
authors.initials: B
authors.lastname: Cao
authors.affiliation: Neuroscience Laboratory, Department of Biology and Chemistry, Centre for Biosystems, Neuroscience, and Nanotechnology, City University of Hong Kong, Hong Kong, China Key Laboratory of Biochip Technology, Shenzhen Biotech and Health Centre, City University of Hong Kong, Shenzhen 518057, PR China.
authors.forename: Jin
authors.initials: J
authors.lastname: Liu
authors.affiliation: Neuroscience Laboratory, Department of Biology and Chemistry, Centre for Biosystems, Neuroscience, and Nanotechnology, City University of Hong Kong, Hong Kong, China Key Laboratory of Biochip Technology, Shenzhen Biotech and Health Centre, City University of Hong Kong, Shenzhen 518057, PR China.
authors.forename: Ying
authors.initials: Y
authors.lastname: Li
mesh_terms: D000707:Anaphylaxis / Q000503:physiopathology*; D000818:Animals; D054732:Calcium-Calmodulin-Dependent Protein Kinase Type 2 / Q000037:antagonists & inhibitors / Q000378:metabolism; D004195:Disease Models, Animal; D004558:Electric Stimulation; D004567:Electrodes, Implanted; D018691:Excitatory Amino Acid Antagonists / Q000494:pharmacology; D058787:GABA-A Receptor Antagonists / Q000494:pharmacology; D006179:Gyrus Cinguli / Q000187:drug effects / Q000503:physiopathology*; D008297:Male; D018482:Muscle, Skeletal / Q000187:drug effects / Q000503:physiopathology; D009434:Neural Pathways / Q000187:drug effects / Q000502:physiology; D009473:Neuronal Plasticity / Q000187:drug effects / Q000502:physiology*; D017207:Rats, Sprague-Dawley; D011963:Receptors, GABA-A / Q000378:metabolism; D017470:Receptors, Glutamate / Q000378:metabolism; D016194:Receptors, N-Methyl-D-Aspartate / Q000037:antagonists & inhibitors / Q000378:metabolism; D013569:Synapses / Q000187:drug effects / Q000502:physiology; D009435:Synaptic Transmission / Q000187:drug effects / Q000502:physiology*; D013788:Thalamus / Q000187:drug effects / Q000502:physiology; D059265:Visceral Pain / Q000503:physiopathology*
chemical_list: D018691:Excitatory Amino Acid Antagonists; D058787:GABA-A Receptor Antagonists; C121001:NR2B NMDA receptor; D011963:Receptors, GABA-A; D017470:Receptors, Glutamate; D016194:Receptors, N-Methyl-D-Aspartate; D054732:Calcium-Calmodulin-Dependent Protein Kinase Type 2
keywords: anterior cingulate cortex; basal synaptic transmission; long-term potentiation; medial thalamus; visceral hypersensitivity